<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ju C</submitter><funding>The Everest Project of Fourth Military Medical University</funding><funding>Shaanxi Provincial Key R&amp;D Program</funding><funding>Shaanxi Provincial Key R&amp;amp;D Program</funding><funding>National Natural Scientific Foundation of China</funding><funding>Discipline Boost Project of the First Affiliated Hospital of Air Force Military Medical University</funding><pagination>5</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9854040</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>28(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Secondary spinal cord injury (SCI) often causes the aggravation of inflammatory reaction and nerve injury, which affects the recovery of motor function. Bone-marrow-derived macrophages (BMDMs) were recruited to the injured area after SCI, and the M1 polarization is the key process for inducing inflammatory response and neuronal apoptosis. We previously showed that photobiomodulation (PBM) can inhibit the polarization of M1 phenotype of BMDMs and reduce inflammation, but the underlying mechanisms are unclear. The purpose of this study is to explore the potential target and mechanism of PBM in treating SCI.&lt;h4>Methods&lt;/h4>Transcriptome sequencing and bioinformatics analysis showed that long noncoding RNA taurine upregulated gene 1 (lncRNA TUG1) was a potential target of PB</pubmed_abstract><journal>Cellular &amp; molecular biology letters</journal><pubmed_title>Photobiomodulation promotes spinal cord injury repair by inhibiting macrophage polarization through lncRNA TUG1-miR-1192/TLR3 axis.</pubmed_title><pmcid>PMC9854040</pmcid><funding_grant_id>NO.2020ZDLSF02-05</funding_grant_id><funding_grant_id>2018RCFC02</funding_grant_id><funding_grant_id>XJZT19Z22</funding_grant_id><funding_grant_id>NO.2021ZDLSF02-10</funding_grant_id><funding_grant_id>NO.81572151</funding_grant_id><funding_grant_id>NO.81070996</funding_grant_id><funding_grant_id>XJZT21L01</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Zhu Z</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Ding T</pubmed_authors><pubmed_authors>Zuo X</pubmed_authors><pubmed_authors>Liang Z</pubmed_authors><pubmed_authors>Hu X</pubmed_authors><pubmed_authors>Ma Y</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Ju C</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Song Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Photobiomodulation promotes spinal cord injury repair by inhibiting macrophage polarization through lncRNA TUG1-miR-1192/TLR3 axis.</name><description>&lt;h4>Background&lt;/h4>Secondary spinal cord injury (SCI) often causes the aggravation of inflammatory reaction and nerve injury, which affects the recovery of motor function. Bone-marrow-derived macrophages (BMDMs) were recruited to the injured area after SCI, and the M1 polarization is the key process for inducing inflammatory response and neuronal apoptosis. We previously showed that photobiomodulation (PBM) can inhibit the polarization of M1 phenotype of BMDMs and reduce inflammation, but the underlying mechanisms are unclear. The purpose of this study is to explore the potential target and mechanism of PBM in treating SCI.&lt;h4>Methods&lt;/h4>Transcriptome sequencing and bioinformatics analysis showed that long noncoding RNA taurine upregulated gene 1 (lncRNA TUG1) was a potential target of PB</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-06-21T03:18:55.662Z</modification><creation>2025-02-19T01:08:19.291Z</creation></dates><accession>S-EPMC9854040</accession><cross_references><pubmed>36658478</pubmed><doi>10.1186/s11658-023-00417-0</doi></cross_references></HashMap>